Influence of continuous rotation or reciprocation of Optimum Torque Reverse motion on cyclic fatigue resistance of nickel-titanium rotary instruments.

AIM: To evaluate the resistance to cyclic fatigue of ProTaper Next (PTN; Dentsply Sirona, Ballaigues, Switzerland), Revo-S (Micro-Mega, Besançon, France), Mtwo (Sweden & Martina, Padova, Italy), Twisted Files (TF, SybronEndo, Orange, CA, USA) and EndoWave (J Morita Corporation, Osaka, Japan) used in continuous rotation or in reciprocation of Optimum Torque Reverse motion (OTR). METHODOLOGY: A total of 120 nickel-titanium files were tested. Twenty-four instruments for each brand were divided into two groups (n = 12) on the basis of the motion tested: continuous rotation (Group 1) or reciprocation of OTR motion (Group 2). Resistance to cyclic fatigue was determined by recording time to fracture (TtF) in a stainless steel artificial canal with a 60° angle of curvature and 5 mm radius of curvature. The TtF data were analysed by using two-way analysis of variance (anova) and Bonferroni's post hoc tests at 0.05. RESULTS: Mtwo and TF had significantly higher TtF when compared with all other instruments, both in continuous rotation and in reciprocation of OTR motion (P < 0.0001 and P < 0.05, respectively). No difference was observed between Mtwo and TF (P > 0.05), in both motions. PTN was associated with higher cyclic fatigue resistance than Revo-S and EndoWave, both in continuous rotation and in reciprocation of OTR motions (P < 0.0001). No difference was observed between Revo-S and EndoWave, in both motions (P > 0.05). Reciprocating OTR motion improved TtF of all instruments (P < 0.0001). CONCLUSIONS: Reciprocation of OTR motion improved significantly cyclic fatigue resistance of all instruments tested compared with continuous rotation. Mtwo and TF had significantly higher cyclic fatigue than the other instruments, in both continuous rotation and reciprocation of OTR motion.

Atherosclerosis: analysis of the eNOS (T786C) gene polymorphism.

The coronary arteriosclerotic disease is the most common cardiovascular disease. Atherosclerosis affects large- and medium-sized arteries leading to severe thrombosis or artery stenosis that could evolve to myocardial infarction, ischemic stroke, ischemic injury of kidneys and intestines, and several other life-threatening clinical manifestations. Nitric oxide has been shown to be a promising therapeutic agent against cardiovascular diseases. The eNOS gene assumes several important functions, including regulation of vascular tone and regional blood flow, the suppression of vascular smooth muscle cell proliferation, and modulation of leukocyte-endothelium interactions. The T786C polymorphism is an important point mutation, where thymine is changed to cytosine. T786C significantly reduces the activity of the eNOS promoter gene. Two hundred and ninety-seven peripheral blood samples were collected from patients with the previous diagnosis of atherosclerotic disease based on clinical examination and confirmed by imaging methods. Results were compared using the chi-square test and the G-test. In the present study, the TC genotype was more frequent in both case and control groups with no statistically significant difference. Comparing the relation TC/TT and CC genotypes in the case and control groups, there was no statistically significant difference. No significant difference was found when genotypes were analyzed regarding gender and smoking. Our results suggest a strong tendency of the T allele, in single or double dose, to be associated with atherosclerosis that was not confirmed by the scientific data.

Analysis of p53 gene polymorphism (codon 72) in symptomatic patients with atherosclerosis.

Atherosclerosis is a multifactorial pathological disease that alters the morphology and function of arterial walls. The atheroma growth leads to vessel hardening and lumen narrowing, limiting the blood flow. The atheroma plaque can eventually break, expose highly thrombogenic material and lead to platelet activation and subsequent formation of a thrombus that may block blood flow in loco, or even leading to obstruction of other vessels with a smaller diameter. This process is one of the main determinants of the clinical manifestations of atherosclerosis, such as coronary artery disease, ischemic stroke, and peripheral arterial disease. Although the inflammatory theory about atherosclerosis is the most renowned one, observations point to common biological characteristics between cancer and atherosclerosis suggesting a possible association between p53 and atherosclerotic diseases. We collected peripheral blood samples from 200 individuals with clinical manifestations of atherosclerotic disease and 100 individuals without manisfestation of the disease to form the control group. DNA was subjected to molecular analysis (PCR) to identify the polymorphism of the p53 gene. We have not found any relationship between the polymorphism of the p53 gene and atherosclerosis in the population studied (P = 0.36). There was no relationship between atherosclerosis, polymorphism of p53 and the variables accounted: smoking habit (P = 0.72, 0.51 and 0.62 for smokers, non-smokers and former smokers respectively), alcohol consumption (P = 0.17 for individuals with drinking habits and 0.38 for those who do not consume alcohol beverage), systemic arterial hypertension (P = 0.60), diabetes mellitus (P = 0.34), and dyslipidemia (P = 0.89). Our population has a high rate of miscegenation and heterozygotes, and according to studies the arginine variant is more related to plaque formation because it induces apoptosis more frequently when compared to the proline variant. According to our results, there is no association between the polymorphism of the p53 gene, atherosclerosis and its risk factors in the population studied.

Molecular analysis of the GSTT1 gene polymorphism in patients with clinical manifestation of atherosclerosis.

Atherosclerosis is a chronic inflammatory disease formed by the accumulation of lipids in the innermost layer and large-caliber artery (tunica intima). This accumulation, along with platelet factors, stimulates the proliferation of muscle cells in this region. Over than 400 genes may be related to the pathology since they regulate endothelial function, coagulation, inflammation, metabolism of amino acids, lipids, and carbohydrates. Glutathione S-transferases (GST) are enzymes that catalyze the polymorphic detoxification of metabolites produced by oxidative stress within the cells, which is induced by reactive oxygen species. GSTs are one of the defense mechanisms against oxidative stress damage. Due to genetic, cultural, and environmental factors, the rate of atherosclerosis is higher; however, an early diagnosis is crucial for the prevention and treatment of several complications related to the disease. The present study aimed to analyze the frequency of GSTT1 genotypes regarding the presence or absence of the polymorphism in patients with clinical manifestation of atherosclerosis. We collected 200 samples of peripheral blood of patients with the previous diagnosis of atherosclerosis based on clinical examination and imaging, and 100 samples of peripheral blood to compose the control group of patients without clinical manifestation of atherosclerosis. The polymorphism was assessed by PCR and analyzed on the agarose gel stained with 2.0% ethidium bromide. The frequency of the GSTT1 gene polymorphism was compared using the chi-square test (P < 0.05) and the G-test. In the case group, we detected 85.5% of patients with the GSTT1 genotype present and 14.5% of patients with the null genotype. A significant difference was observed between groups (case vs control) for the presence of the GSTT1 polymorphism. According to the analysis of the variable alcohol consumption, we found that in the case group the presence of the GSTT1 gene was higher in individuals who reported not drinking alcohol. In this study, the presence of the GSTT1 gene polymorphism in male patients with atherosclerosis was 1.5 times higher when compared to female patients. Regarding the variable time of smoking, we found that this genotype was more frequent in smokers for both case and control groups.

Polymorphism of the gene eNOS G894T (Glu298Asp) in symptomatic patients with aterosclerosis.

Atherosclerotic and its cardiovascular complications are responsible for 17.5 million deaths a year, according to the World Health Organization. There is consensus that atherosclerosis involves multiple pathogenic processes initiated by endothelial dysfunction, with inflammation and vascular proliferation determining alterations in the matrix, with consequent formation of the atheromatous plaque and its clinical implications. Risk factors such as hypertension, diabetes mellitus, dyslipidemia, and smoking are widely known. Currently, genotyping, which is not directly related to these factors, is not accepted to estimate the risk of cardiovascular diseases, but strong evidence indicates several polymorphic genes as factors of risk and progression leading to complications of the disease. Among the genes involved, eNOS (endothelial nitric oxide synthase gene), which is responsible for the production of endothelial nitric oxide (an important arterial vasodilator), when presented in polymorphic variation can determine production, malfunction, and predisposition to atherosclerosis. In the present study, we analyzed the G894T polymorphism of the eNOS gene in groups of individuals diagnosed with atherosclerosis and in a control group. We collected 200 blood samples from patients previously diagnosed with atherosclerosis and 100 samples formed the control group. The genotyping analysis for polymorphism of the eNOS gene was determined by PCR. We considered variables such as gender, smoking, smoking history, and alcohol consumption; statistical differences were found in the distribution of case and control groups (P = 0.0378) and in non-smoking patients (P = 0.0263). In the other associations, no statistically significant difference was found. In the population studied, the frequency of the heterozygous genotype (GT) was much higher than in the other populations (GG and TT) in both groups (case and control). The GG genotype showed greater susceptibility to atherosclerosis. Association of the GG genotype in non-smokers also showed greater susceptibility. Gender, alcohol consumption, smoking, and smoking history did not influence atherosclerosis.

GSTM1 polymorphism in patients with clinical manifestations of atherosclerosis.

Atherosclerosis is characterized by lesions, called atheroma or atheromatous plaques, in the inner layer of blood vessels, which block the vascular lumen and weaken the underlying tunica media. Several modifiable and non-modifiable risk factors for the development of atherosclerosis exist. The modifiable risk factors include hypertension, smoking, obesity, high LDL and low HDL cholesterol levels, sedentary lifestyle, and stress; the non-modifiable factors include diabetes mellitus, family history of hypertension and heart disease, thrombophilia, sex, age, and genetic factors. The association of polymorphisms in GST with coronary artery disease has been studied since the polymorphisms can affect enzyme activity and contribute to the onset of atherosclerosis. We analyzed polymorphisms in GSTM1 in individuals diagnosed with atherosclerosis as well as in healthy individuals (control group). The frequency of the GSTM1 present genotype in the atherosclerosis group was 1.2 times higher than that observed in the control group. We found no sex- or alcohol-consumption-dependent differences between the occurrences of the present and null genotypes. However, the GSTM1 present genotype occurred in 52.6% individuals with atherosclerosis who reported smoking 20 or more cigarettes per day and in 60% individuals who smoked 10 to 20 cigarettes per day (P = 0.0035). In addition, the GSTM1 present genotype was more frequent in individuals who reported being former smokers - 45.5% in individuals with atherosclerosis who smoked for more than 20 years and 50% each for individuals in the control group who smoked for less than 10 years or for 10 to 20 years, respectively (P = 0.0240).

Clinical and microbiological effects of adjunctive antibiotics in treatment of localized juvenile periodontitis. A controlled clinical trial.

The aim of this study was to assess the clinical and microbiologic effects of the combination of amoxicillin and metronidazole therapy as an adjunct to mechanical treatment in the management of localized juvenile periodontitis. Twenty-five localized juvenile periodontitis (LJP) patients from a Brazilian population were randomly allocated into an experimental group receiving mechanical treatment and antibiotics, and a control group receiving mechanical treatment and placebo. Clinical and radiographic assessments, as well as microbiologic sampling for Actinobacillus actinomycetemcomitans, were performed at baseline and one year after the end of the treatment. At the termination of the study A. actinomycetemcomitans could be isolated from the oral cavity of all patients in the control group who harbored the bacterium at baseline and in 4 out of 8 patients in the experimental group. Both treatment modalities resulted in significant benefit on an individual basis. The experimental group, however, displayed better results than did the control group regarding gingival index (GI), probing depth (PD), clinical attachment level (CAL), and radiographic analysis of crestal alveolar bone mass, but not with respect to plaque index (PI). No serious adverse effects of the antibiotic treatment were observed in the present study.

Localized juvenile periodontitis and Actinobacillus actinomycetemcomitans in a Brazilian population.

Localized juvenile periodontitis (LJP) has been used as a model for studying periodontal disease, and its prevalence is considered to be higher in third-world countries (0.3-8%) than in industrialized countries (0.1%). Mostly, the disease has been associated with Actinobacillus actinomycetemcomitans (A.a.) but lack of association has also been reported. The aim of this study was to identify LJP patients in geographically different Brazilian populations and assess the presence of A.a. in their periodontal lesions. 7843 children, 12-19-years of age, from the cities of Rio de Janeiro, Votorantim and Belo Horizonte were screened, and LJP patients were identified by strict clinical and radiographical criteria. A final LJP prevalence of 0.3%, with a 99% confidence interval between 0.16% to 0.47%, was found. The prevalence in the subpopulations varied between 0.1-1.1% in the different areas. Subgingival bacterial samples were obtained from the oral cavity of 25 patients and their family members. 80% of these patients, 39.5% of their family members, 35.3% of their parents, and 43.9% of all siblings were culture positive for A.a. All but one of the families had at least one member in addition to the patient who was culture positive for A.a. In 3 families, > 1 member showed radiographic and clinical signs of LJP. 30% of non-LJP subjects coming from one of the areas with higher LJP prevalence harbored A.a. We conclude that LJP is highly associated with A.a. in this Brazilian population.